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Basics ⬇

Outline

BASICS

Definition!!navigator!!

  • EMS is a collection of risk factors for laminitis that includes ID, generalized obesity and/or regional adiposity, dyslipidemia, and altered adipokine concentrations
  • Insulin abnormalities detected in equids with EMS include fasting hyperinsulinemia, excessive insulin responses to oral sugars, and insulin resistance. These problems are collectively referred to as ID

Pathophysiology!!navigator!!

  • EMS results from an interaction between genetics and environment, and the risk of laminitis in the individual animal depends on both genetic and environmental influences. Consumption of high-sugar feeds, obesity, and PPID are exacerbating factors
  • Hyperinsulinemia occurs in affected horses and increases the risk of laminitis developing. Laminitis has been experimentally induced in horses by infusing high doses of insulin IV. The risk of laminitis is likely to increase as blood insulin concentrations increase. Mechanisms involved in hyperinsulinemia-induced laminitis include binding of insulin to insulin-like growth factor-1 receptors and altered blood flow or endothelial cell function within the hoof vessels as a result of hyperinsulinemia
  • Incretin hormones (glucagon-like peptide-1 and glucose-dependent insulinotropic peptide) likely play a role in EMS. Both hormones are secreted by intestinal cells in response to amino acids and sugars, and stimulate the release of insulin from pancreatic beta cells

Systems Affected!!navigator!!

Genetics!!navigator!!

Genetic component of EMS in Morgan horses, Arabians and Welsh ponies.

Incidence/Prevalence!!navigator!!

  • Pasture-associated laminitis accounts for approximately 45% of laminitis cases occurring on United States farms
  • Laminitis episodes occur more frequently in the spring as pastures turn green. Episodes also occur when the grass is challenged by dry conditions, growing quickly after summer rains, or adapting to the cooler temperatures of the fall season

Geographic Distribution!!navigator!!

EMS may be more common in regions with heavier rainfall and greener pastures. Geographic distribution of EMS is unknown.

Signalment!!navigator!!

  • Predisposed breeds include Morgan horses, Paso Fino, Andalusian, and pony breeds. Arabian, Quarter Horse, Saddlebred, Tennessee Walking Horse, and Warmblood breeds of horse are also affected. Standardbreds and Thoroughbreds are less likely to be affected
  • EMS may only be recognized when a horse becomes middle aged
  • Hyperinsulinemia may be exacerbated by PPID
  • No known sex predilection

Signs!!navigator!!

  • Many horses with EMS exhibit generalized obesity and/or regional adiposity, but others have a leaner phenotype and can only be identified by testing for ID
  • Regional adiposity, including a “cresty neck” and/or fat deposits next to the tail-head, in the sheath, within the supraorbital fossae, or randomly distributed throughout the trunk region as subcutaneous masses
  • Divergent growth rings that are wider at the heel than the toe (founder lines) may indicate historical laminitis and may be detected in horses that do not have a history of lameness
  • “Easy keepers”

Causes!!navigator!!

  • Environmental factors include high NSC diet (e.g. concentrates or pasture with abundant grass) and insufficient exercise
  • Laminitis episodes are likely be triggered by hyperinsulinemia

Risk Factors!!navigator!!

  • See Genetics
  • Offspring of a mare or stallion with EMS
  • “Easy keeper”

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Some horses can be obese without ID
  • PPID (also called equine Cushing disease) is distinguished from EMS by the presence of muscle wasting, an increased caloric requirement to maintain body mass, and delayed haircoat shedding. PPID has a higher frequency in aged horses

CBC/Biochemistry/Urinalysis!!navigator!!

  • Blood glucose concentrations may be high normal
  • Mildly increased triglyceride concentrations (hypertriglyceridemia)
  • Mildly increased γ-glutamyltransferase concentrations
  • Glucosuria is not detected unless diabetes mellitus has developed

Other Laboratory Tests!!navigator!!

  • Serum or plasma insulin concentrations—blood can be collected when hay is available or as horses graze on pasture, but do not feed grain within 4 h of sample collection. Fasting is no longer recommended. Interpretation—no evidence of ID if insulin concentration <20 μU/mL (also written as mU/L); ID suspected if 20–50 μU/mL; and ID is present if the insulin is >50 μU/mL. Suspect horses with insulin values <20 μU/mL should undergo further testing to rule out ID. Concentrations may be reported in pmol/L and the conversion factor is approximately 7
  • Serum leptin concentrations—increased in equids with EMS due to increased body fat
  • High-molecular-weight adiponectin—decreased in equids with EMS, and this variable may be useful for assessing laminitis risk

Imaging!!navigator!!

Horses with EMS often show radiographic evidence of laminitis, including rotation and bony remodeling of the third phalanx. These abnormalities may be detected in the absence of any discernable lameness and provide evidence of prior subclinical laminitis events.

Other Diagnostic Procedures!!navigator!!

OST—often used to detect ID. Withhold feed for 3–8 h before testing. It is common practice to leave 1 flake of hay with the horse after 10:00 PM and then withhold feed until the test is completed the following morning. Administer 0.15 mL Karo Light syrup per kilogram body weight (75 mL for a 500 kg horse) orally via a dose syringe and collect blood at 60–90 min. Measure insulin and glucose concentrations. An insulin concentration >45 μU/mL provides evidence of ID. Glucose values are assessed to detect diabetes mellitus, which may occur in horses with EMS. Other glucose or insulin tolerance tests are available (see chapters Glucose tolerance tests and Insulin levels/insulin tolerance test).

Pathologic Findings!!navigator!!

  • Regional adiposity, including enlarged adipose tissue deposits in the neck region or distributed throughout the subcutaneous tissues as masses
  • Gross or histopathologic evidence of laminitis is often present

Treatment ⬆ ⬇

Outline

TREATMENT

Aims!!navigator!!

  • Weight loss in horses with generalized obesity
  • Improve insulin sensitivity through weight loss, diet, and exercise
  • Avoid dietary triggers for laminitis

Nursing Care!!navigator!!

See chapter Laminitis.

Diet!!navigator!!

  • Obese horses that are easy keepers can be placed on a diet of hay and a vitamin/mineral supplement
  • Obese horses can be fed 1.5% of ideal body weight in hay to induce weight loss
  • Hay fed to EMS horses should have a lower (<12%) NSC content. Samples can be tested by commercial laboratories. Hay with NSC content >12% should be soaked in cold water for 30 min to lower the sugar content
  • Horses with EMS should be supplemented with 1000 IU vitamin E daily
  • Avoid feeds that exacerbate hyperinsulinemia. Restrict or eliminate pasture access, or use a grazing muzzle if on pasture
  • Thinner EMS horses may be supplemented with low-sugar/low-starch feeds

Client Education!!navigator!!

  • Obesity is likely to be an important risk factor for EMS. In obese horses, limit dietary intake, increase exercise, and limit pasture access, particularly at high-risk times of the year
  • Body condition scoring should be routinely performed
  • Development of regional adiposity (e.g. cresty neck) should prompt diagnostic testing for ID
  • PPID is thought to exacerbate ID and increase the risk of laminitis

Surgical Considerations!!navigator!!

In some cases of severe, chronic laminitis, dorsal hoof wall resection and deep digital tenotomy.

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • Levothyroxine sodium (Thyro-L; Vet-A-Mix, Lloyd, Inc., Shenandoah, IA) 12 mg/5 mL (1 teaspoon)
  • Used when rapid weight loss is required in a horse that has suffered from laminitis and is threatened by subsequent episodes, and in horses that remain obese despite stringent diet and exercise interventions
  • Administered at a dosage of 0.1 mg/kg body weight every 24 h, which is equivalent to a total dose of 48 mg or 20 mL (4 teaspoons) daily for a 500 kg horse, administered by mouth or in the feed for 3–6 months
  • Serum thyroxine concentrations are usually between 60 and 100 ng/mL in treated horses. This range can be targeted when lower dosages are selected for smaller patients
  • Taper carefully—halve the dose for 2 weeks and then halve again for 2 weeks in order to allow endogenous thyroid hormone production to resume
  • Metformin hydrochloride 500 mg or 1000 mg tablets
  • Used to blunt the increase in insulin concentrations that follows ingestion of sugars
  • Indicated when hyperinsulinemia persists after obesity has been addressed, PPID managed (if present), and dietary changes have been made
  • Administer 30–60 min before feeding. Starting dosage of 30 mg/kg body weight orally 2 or 3 times daily, depending on feeding schedule. Can be increased to 50 mg/kg every 8–12 h orally in refractory cases
  • Treatment of PPID is indicated if this endocrine disorder has developed

Contraindications!!navigator!!

  • The levothyroxine dosages recommended above are not appropriate for thin horses with ID because weight loss will be induced
  • Neither treatment has been evaluated in pregnant mares

Precautions!!navigator!!

  • Cardiac hypertrophy and bone resorption have been associated with levothyroxine sodium use in humans, but not horses
  • Metformin can cause oral irritation, especially when administered at higher dosages

Possible Interactions!!navigator!!

No known interactions.

Alternative Drugs!!navigator!!

Supplements that are thought to improve insulin sensitivity are also available to horse owners.

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

  • An OST should be repeated after diet, exercise, or treatment interventions
  • Patients should be reevaluated at different times of the year because seasonal and dietary influences vary

Prevention/Avoidance!!navigator!!

  • Avoid overfeeding
  • Regular exercise
  • Currently, it is only possible to recognize that the offspring of affected horses may be predisposed to EMS, but genetic tests may be available in the future

Possible Complications!!navigator!!

Chronic damage to the hoof laminae and structures of the foot.

Expected Course and Prognosis!!navigator!!

EMS is a manageable condition if recognized.

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

N/A

Age-Related Factors!!navigator!!

N/A

Zoonotic Potential!!navigator!!

N/A

Pregnancy/Fertility/Breeding!!navigator!!

N/A

Synonyms!!navigator!!

  • Insulin resistance syndrome
  • Peripheral Cushing syndrome

Abbreviations!!navigator!!

  • EMS = equine metabolic syndrome
  • ID = insulin dysregulation
  • NSC = nonstructural carbohydrates
  • OST = oral sugar test
  • PPID = pituitary pars intermedia dysfunction

Internet Resources!!navigator!!

Equine Endocrinology Group, Equine metabolic syndrome. http://sites.tufts.edu/equineendogroup/equine-metabolic-syndrome/

Suggested Reading ⬆ ⬇

Menzies-Gow NJ, Harris PA, Elliott J. Prospective cohort study evaluating risk factors for the development of pasture-associated laminitis in the UK. Equine Vet J 2017;49(3):300–306.

Schuver A, Frank N, Chameroy KA, et al. Assessment of insulin and glucose dynamics by using an oral sugar test in horses. J Equine Vet Sci 2014;34:465–470.

Author(s) ⬆

Author: Nicholas Frank

Consulting Editors: Michel Lévy and Heidi Banse